Download Questions for Sections D and E

Special Instructions: Not all of the questions that follow were
addressed during the class or laboratory in the Fall 2007
Physiology course. Nevertheless, the topics listed below are very
important and will be included on the tests. Use these questions to
determine which topics should be emphasized as you study.
Chapter 12 Section D
1. What is the formula for Mean Arterial Pressure?
2. How is it possible for blood flow to increase to some organs and yet there be no
change in MAP?
3. How do arterioles contributed to Mean Arterial Pressure?
4. Blood flow through the pulmonary circuit is the same as Q through the systemic
circuit, which means that the cardiac output is the same for the left and right
ventricles. How is it that the MAP in the pulmonary circuit is so dramatically
lower that that of the systemic circuit?
5. Although not directly addressed in this section, consider which of the Starling
forces in the pulmonary capillaries accounts for fact that filtration does not
normally occur at any point along a pulmonary capillary?
6. What reflex is responsible for regulating MAP on a time scale of minutes to
hours?
7. Where are the receptors which sense arterial pressure?
8. As blood pressure rises, how is the frequency of action potentials in the
baroreceptor afferent axons affected?
9. Where is the integrator in the negative feedback loop for blood pressure?
10. How is the secretion of vasopressin affected by a drop in blood pressure?
11. How is the concentration of Angiotensin II affected by a drop in blood pressure?
12. What are the target cells of vasopressin and what effect does vasopressin have
upon those cells? How does the response affect TPR and blood pressure?
13. What are the target cells of vasopressin and what effect does vasopressin have
upon those cells? How does the response affect TPR and blood pressure?
The following questions are based upon the Hemorrhage case described in class.
14. In the initial events of hemorrhage (prior to the responses produced by the
baroreceptors) how is venous return, end-diastolic volume, stroke volume, and
cardiac output affected?
15. How is MAP affected by hemorrhage?
16. By what two mechanisms is heart rate increased in response to hemorrhage?
17. Which neurotransmitters and hormones are responsible?
18. By what mechanism is cardiac contractility increased in response to hemorrhage?
What are neurotransmitter and/or hormone is involved?
19. What accounts for the rapid shallow pulse associated with hemorrhage?
20. What accounts for the cold clammy skin in a person who is hemorrhaging?
Which division of the autonomic nervous system is responsible. Which
neurotransmitters and/or hormone is involved?
21. By what pathways is arteriolar smooth muscle stimulated to contract? Which
neurotransmitters and hormones are involved? What is the effect on TPR?
22. How is venoconstriction brought about during the response to hemorrhage? By
what sequence of steps is cardiac output increased by venoconstriction?
23. What are the components of the negative feedback loop that are responsible for
the production of new erythrocytes to eventually restore hematocrit to normal in
the weeks after a hemorrhage? Be sure to identify the stimulus, the integrator, the
efferent pathway, the effectors and their response.
24. How are Starling forces responsible for the bulk flow of intracellular fluid to the
plasma during a hemorrhage? How would this fluid shift affect hematocrit?
25. Would a person who is recovering from a hemorrhage have blood pressure in the
normal range? Why or why not?
26. Because baroreceptors adapt to the prevailing MAP over a few day, there must be
some other mechanism that is responsible for the long term regulation of MAP.
What is that mechanism and how are the kidneys involved?
Returning now to the text in Section D, p. 444.
27. What other stimuli can cause an increase in MAP?
28. How does visceral or joint pain affect MAP?
29. What observations demonstrate that the set point for blood pressure can be altered
during certain conditions?
30. Describe Cushing’s phenomenon, a positive feedback pathway that develops in
response to elevated intracranial pressure.
Chapter 12 Section E
Consider Figure 12-58 p. 446 when answering these questions. The figure consists of
three phases: prior to hemorrhage, immediately after the massive loss of blood which
precedes the reflex response, and the phase during which the baroreceptor reflex is
orchestrating reflex compensations.
1. Relative to stroke volume prior to hemorrhage, is the stroke volume during the
response to hemorrhage increased or decreased?
2. Relative to heart rate prior to hemorrhage, is the HR during the response to
hemorrhage increased or decreased?
3. Relative to cardiac output prior to hemorrhage, is the CO during the response to
hemorrhage increased or decreased?
4. Relative to total peripheral resistance prior to hemorrhage, is TPR during the
response to hemorrhage increased or decreased?
5. Relative to mean arterial pressure prior to hemorrhage, is MAP during the
response to hemorrhage increased or decreased?
Returning now to the text in Section E.
6. What is autotransfusion?
7. What is erythropoiesis?
8. Hypotension can also be the result of what other conditions?
9. Dr. Davis faints about 50% of the time that he has blood drawn from the
antecubital vein near the elbow. What is the pathway by which this fainting
(syncope) is produced?
10. Severe allergic reactions result in the massive release of vasodilators, especially
histamine. The condition is called low resistance shock. Victims are often treated
with an injection of epinephrine (via an EPI pen.) How does the EPI prevent
further reduction in blood pressure in these patients? (Consider the target cells of
EPI and the effect of EPI on these cells.)
11. What is shock?
12. How does cardiogenic shock differ from hypovolemic shock?
13. Why does a persons sometime feel faint when standing up suddenly?
14. If you must stand still for a long time, what can you do to prevent fainting caused
by pooling of blood in veins below the heart?
Cardiovascular Responses during Exercise
15. During exercise, how is blood flow to each of the following affected: skin, heart,
kidney, intestines, skeletal muscle.
16. During exercise, does TPR increase or decrease? Explain.
17. During exercise, how is CO increased?
18. During exercise, MAP is only slightly increased even though CO is dramatically
increased (from 5L/min to 30 L/min). What accounts for the relatively small
elevation in MAP during exercise?
19. What are the various factors that contribute to the larger stroke volume and heart
rate associated with exercise?
20. What is the “skeletal muscle pump?”
21. What is the “respiratory pump?”
22. During exercise, how is blood flow to skeletal muscles matched to their
metabolism?
23. What effect do mechanoreceptors in exercising muscles have upon the set point
for MAP?
24. What is the explanation that accounts for the huge elevation in blood pressure
during a wrestling match in which wrestlers sustain isometric contractions of long
duration while attempting to pin the opponent? (hint: How is blood flow to a
skeletal muscle affected by contraction of that muscle?)
Hypertension
25. What is the dividing line between normal blood pressure and hypertension?
26. How does hypertension affect “afterload” and how can hypertension lead to
cardiac hypertrophy?
27. Table 12-8 lists the categories of drugs used to treat hypertension. Be familiar
with these categories and their modes of action.
Heart Failure
28. What is heart failure?
29. What is pulmonary edema?
30. Table 12-9 lists drugs used to treat heart failure. Be familiar with these drugs and
their modes of action.
Coronary Artery Disease and Heart Attacks
31. What is ischemia?
32. What is myocardial infarction?
33. What is angina pectoris?
34. What are the symptoms of a heart attach?
35. How can a blood test reveal if a person has experienced a heart attack?
36. What is ventricular fibrillation?
37. What is the goal of defibrillation?
38. What is atherosclerosis?
39. How does atherosclerosis contribute to a heart attack?
40. How is nitroglycerin effective in treating a heart attack?
41. What is the goal of cardiac balloon angioplasty?
42. What is the purpose of a coronary stent?
For 2007, we have insufficient time to cover in class Chapter 12 Section F dealing with
Blood and Hemostasis and therefore this material will not be included in the Physiology
Tests for Fall 2007. However, those students intending to take the MCAT, DCAT or GRE
in preparation for advanced degrees should seriously consider using the supplemental
questions to guide their reading and understanding of this material.